Gender-based crime is one of the most concerning scourges of contemporary society. Governments worldwide have invested lots of economic and human resources to radically eliminate this threat. Despite these efforts, providing accurate predictions of the risk that a victim of gender violence has of being attacked again is still a very hard open problem. The development of new methods for issuing accurate, fair and quick predictions would allow police forces to select the most appropriate measures to prevent recidivism. In this work, we propose to apply Machine Learning (ML) techniques to create models that accurately predict the recidivism risk of a gender-violence offender. The relevance of the contribution of this work is threefold: (i) the proposed ML method outperforms the preexisting risk assessment algorithm based on classical statistical techniques, (ii) the study has been conducted through an official specific-purpose database with more than 40,000 reports of gender violence, and (iii) two new quality measures are proposed for assessing the effective police protection that a model supplies and the overload in the invested resources that it generates. Additionally, we propose a hybrid model that combines the statistical prediction methods with the ML method, permitting authorities to implement a smooth transition from the preexisting model to the ML-based model. This hybrid nature enables a decision-making process to optimally balance between the efficiency of the police system and aggressiveness of the protection measures taken.

Although the protumoral functions of polymorphonuclear neutrophils are well known, some now-forgotten studies report antitumoral roles for these cells. The present work examines the antitumoral effect of maintained neutrophilia induced via the injection of recombinant human granulocyte colony stimulating factor (rhG-CSF, 100 μg/kg/day) in a Panc-1 subcutaneous xenograft murine model of pancreatic cancer. This treatment was compared with gemcitabine administration (120 mg/kg every two days) and a saline control (n = 6–7 mice per group). Compared to the controls, both the rhG-CSF- and gemcitabine-treated mice showed significantly suppressed tumor growth by day 4 (p < 0.001 and p = 0.013 respectively). From a mean starting volume of 106.9 ± 3.1 mm3 for all treatment groups, the final mean tumor volumes reached were 282.0 ± 30.7 mm3 for the rhG-CSF-treated mice, 202.6 ± 18.1 mm3 for the gemcitabine-treated mice and 519.4 ± 62.9 mm3 for the control mice (p < 0.004 and p < 0.01, respectively, vs. control). The rhG-CSF-treated tumors showed higher percentage necrosis than those treated with gemcitabine (37.4 ± 4.6 vs. 7.5 ± 3.0; p < 0.001). This is the first report of a clear anti-tumoral effect of rhG-CSF when used in monotherapy against pancreatic cancer. Since rhG-CSF administration is known to be associated with very few adverse events, it may offer an attractive alternative in the clinical treatment of pancreatic cancer.

Background Peritumoral inflammation—a response mainly involving polimorphonuclear neutrophils—has traditionally been thought protumoral in its effects. In recent years, however, a number of studies have indicated that it may play an important antitumoral role. This discrepancy has been difficult to explain. Methods and findings This work describes a tool for simulating tumor growth that obeys the universal model of tumor growth dynamics, and shows through its use that low intensity peritumoral inflammation exerts a protumoral effect, while high intensity inflammation exerts a potent antitumoral effect. Indeed, the simulation results obtained indicate that a sufficiently strong antitumoral effect can reverse tumor growth, as has been suggested several times in the clinical literature. Conclusions The present result indicate that an ‘immunological threshold’ must exist, marking the boundary between states in which peritumoral inflammation is either harmful or beneficial. These findings lend support to the idea that stimulating intense peritumoral inflammation could be used as a treatment against solid tumors.

When a new type of individual appears in a stable population, the newcomer is typically not advantageous. Due to stochasticity, the new type can grow in numbers, but the newcomers can only become advantageous if they manage to change the environment in such a way that they increase their fitness. This dynamics is observed in several situations in which a relatively stable population is invaded by an alternative strategy, for instance the evolution of cooperation among bacteria, the invasion of cancer in a multicellular organism and the evolution of ideas that contradict social norms. These examples also show that, by generating different versions of itself, the new type increases the probability of winning the struggle for fitness. Our model captures the imposed cooperation whereby the first generation of newcomers dies while changing the environment such that the next generations become more advantageous.

We compare using visibility the usual Kardar-Parisi-Zhang (KPZ) universality class and a fractional Edward-Wilkinson (EWf) equation with correlated noise, which share the same kinetic roughening exponents. The KPZ universality class is described by an equation in terms of the usual derivatives, uncorrelated noise and therefore is intrinsically local. The second model includes fractional powers of the Laplace operator and correlated noise, both of which are nonlocal. From their scaling properties, one could be tempted to conclude that both dynamics belong to the same universality class, specifically, to the KPZ universality class. However, this is a wrong conclusion that calls the attention against the indiscriminate application of this approach in real systems without taking into consideration basic physical assumptions (e.g. locality). These examples reveal the necessity of finding new algorithms for detecting characteristics that remain unnoticed to classical scaling analysis, where only the two first moments of the interface distribution (mean and variance) are used to classify the dynamics. We show that visibility and, in particular, the kinetic roughening exponents of the visibility interface, are able to distinguish between these two dynamics which are confused by standard techniques. (C) 2016 Elsevier B.V. All rights reserved.

Tumor growth is a complex process characterized by uncontrolled cell proliferation and invasion of neighboring tissues. The understanding of these phenomena is of vital importance to establish appropriate diagnosis and therapy strategies and starts with the evaluation of their complexity with suitable descriptors produced by scaling analysis. There has been considerable effort in the evaluation of fractal dimension as a suitable parameter to describe differences between normal and pathological tissues, and it has been used for brain tumor grading with great success. In the present work, several contributions, which exploit scaling analysis in the context of brain tumors, are reviewed. These include very promising results in tumor segmentation, grading, and therapy monitoring. Emphasis is done on scaling analysis techniques applicable to multifractal systems, proposing new descriptors to advance the understanding of tumor growth dynamics in brain. These techniques serve as a starting point to develop innovative practical growth models for therapy simulation and optimization, drug delivery, and the evaluation of related neurological disorders.

We consider growing interfaces as dynamical networks whose nodes are the discrete points of the interface and the edges the physical interactions among them. We map the points of the interface formed at each time into a graph by means of a visibility algorithm. As the corresponding interfaces grow, their visibility graphs change over time. We show that the visibility graphs are all scale free for each time. We use the variance of the node degrees as a measure of the dynamical properties of these graphs. This magnitude reveals an unexpected scaling behaviour of these graphs in both the number of nodes and time. This enables to define three robust exponents that characterize any type of dynamics with more detail than the classical scaling analysis applied directly to the physical interfaces. To check the feasibility of this approach we study and classify six different dynamical processes and estimate their critical exponents. We conclude that the dynamics of physical systems far from equilibrium can be determined by its corresponding visibility network. Indeed, this methodology is able to discern among dynamical processes that hitherto have been classified in the same universality class according to the scaling analysis of their interfaces.

Polymorphonuclear neutrophils (PMN) are the most abundant circulating immune cells and represent the first line of immune defense against infection. This review of the biomedical literature of the last 40 years shows that they also have a powerful antitumoral effect under certain circumstances. Typically, the microenvironment surrounding a solid tumor possesses many of the characteristics of chronic inflammation, a condition considered very favorable for tumor growth and spread. However, there are many circumstances that shift the chronic inflammatory state toward an acute inflammatory response around a tumor. This shift seems to convert PMN into very efficient anticancer effector cells. Clinical reports of unexpected antitumoral effects linked to the prolonged use of granulocyte colony‐stimulating factor, which stimulates an intense and sustained neutrophilia, suggest that an easy way to fight solid tumors would be to encourage the development of intense peritumoral PMN infiltrates. Specifically designed clinical trials are urgently needed to evaluate the safety and efficacy of such drug‐induced neutrophilia in patients with solid tumors. This antitumoral role of neutrophils may provide new avenues for the clinical treatment of cancer. © 2009 Wiley Periodicals, Inc. Med Res Rev, 31, No. 3, 311–363, 2011

Background Mycobacterium tuberculosis is a particularly aggressive microorganism and the host's defense is based on the induction of cellular immunity, in which the creation of a granulomatous structure has an important role. Methodology We present here a new 2D cellular automata model based on the concept of a multifunctional process that includes key factors such as the chemokine attraction of the cells; the role of innate immunity triggered by natural killers; the presence of neutrophils; apoptosis and necrosis of infected macrophages; the removal of dead cells by macrophages, which induces the production of foamy macrophages (FMs); the life cycle of the bacilli as a determinant for the evolution of infected macrophages; and the immune response. Results The results obtained after the inclusion of two degrees of tolerance to the inflammatory response triggered by the infection shows that the model can cover a wide spectrum, ranging from highly-tolerant (i.e. mice) to poorly-tolerant hosts (i.e. mini-pigs or humans). Conclusions This model suggest that stopping bacillary growth at the onset of the infection might be difficult and the important role played by FMs in bacillary drainage in poorly-tolerant hosts together with apoptosis and innate lymphocytes. It also shows the poor ability of the cellular immunity to control the infection, provides a clear protective character to the granuloma, due its ability to attract a sufficient number of cells, and explains why an already infected host can be constantly reinfected.

There is evidence that polymorphonuclear neutrophils (PMNs) can exert severe antineoplastic effects. Cross-talk between tumour cells and endothelial cells (ECs) is necessary for the accumulation of PMN around a tumour. This work reports the ability of two PMN-sensitive, human, permanent cell lines—colorectal adenocarcinoma (HT-29) and pharyngeal squamous-cell carcinoma (FaDu) cells—to act as inflammatory foci. PMNs were cytotoxic to both lines, the adhesion of the PMNs to the tumour cells being important in this effect. The tumour cells released appreciable amounts of IL-8 and GROα, and induced the transmigration of PMN through human microvascular-EC monolayers. Conditioning media associated with both lines induced the adhesion of PMN and the surface expression of ICAM-1 in microvascular-EC. In addition, FaDu-conditioning-medium strongly induced the production of proinflammatory cytokines by microvascular-EC. These results support the idea that tumour cells might normally induce a potent acute inflammatory response, leading to their own destruction.

We have investigated the effects of a carbon monoxide-releasing molecule, tricarbonyldichlororuthenium(II) dimer (CORM-2), on catabolic processes in human osteoarthritis (OA) cartilage and chondrocytes activated with interleukin-1 beta. In these cells, proinflammatory cytokines induce the synthesis of matrix metalloproteinases (MMPs) and aggrecanases, including members of a disintegrin and metalloproteinase with thrombospondin domain (ADAMTS) family, which may contribute to cartilage loss. CORM-2 down-regulated MMP-1, MMP-3, MMP-10, MMP-13, and ADAMTS-5 in OA chondrocytes, and it inhibited cartilage degradation. These effects were accompanied by increased aggrecan synthesis and collagen II expression in chondrocytes. Our results also indicate that the inhibition of extracellular signal-regulated kinase 1/2 and p38 activation by CORM-2 may contribute to the maintenance of extracellular matrix homeostasis. These observations suggest that CORM-2 could exert chondroprotective effects due to the inhibition of catabolic activities and the enhancement of aggrecan synthesis.

HCCK the B max values being 121550±45550 and 84880±5380 sites/cell, respectively.From these data the calculated K D values were 1.1±0.06(HFLS) and 3.1±1.7 (HCCK) nM.Inhibition curves were performed with antagonists (1 pM-1 mM) or unlabelled BK at the [ 3 H]BK binding (1.5 nM).K i values for BK were 0.93±0.12(HFLS) and 0.83±0.12(HCCK) nM.Both antagonists displayed high affinity values: MEN16132 K i values of 1.35±0.05and 1.75±0.35nM in HFLS and HCCK, respectively, and icatibant was 3-to 5-fold less potent, K i values being 4.6±1.7 and 8.8±2.9 nM.BK induced IP accumulation both in HFLS (EC 50 0.73±0.08nM) and HCCK (EC 50 0.64±0.05nM), and the induced maximal effect was 11±3 (HFLS) and 15±1.5 (HCCK) fold over the basal response.The antagonists potency was evaluated by preincubating cells with MEN16132 or icatibant at different concentrations (0.1 nM-10 mM) for 15 min before the agonist concentration-response curve (0.03 nM-100 mM).Both antagonists displayed a concentration-dependent antagonism, by shifting to the right the BK curve, but MEN16132 displayed a greater potency in respect to icatibant.The calculated pK B values were 9.93±0.09(HFLS) and 10.44±0.16(HCCK) for MEN16132, and 8.1±0.03(HFLS) and 8.2±0.16(HCCK) for icatibant.Conclusions: This is the first study quantifying B 2 receptors, the affinity and potency of BK and its antagonists in HCCK.Current data highlight the pharmacological profile of MEN16132 as a very potent bradykinin antagonist, in respect with icatibant, both in HFLS and HCCK.

Tumour growth can be described in terms of mathematical models from different points of view due to its multiscale nature. Dynamic scaling is a heuristic discipline that exploits the geometrical features of growing fronts using different concepts from the theory of stochastic processes and fractal geometry. This work is concerned with some problems that arise in the study of tumour–host interfaces. The behaviour of their fluctuations leads to some stochastic evolution equations, which are studied here in the radial symmetry case. Some questions concerning the dynamic scaling of these models and their comparison with experimental results are addressed.

Although the complex and multifactorial process of tumour growth has been extensively studied for decades, our understanding of the fundamental relationship between tumour growth dynamics and genetic expression profile remains incomplete. Recent studies of tumour dynamics indicate that gene expression in solid tumours would depend on the distance from the centre of the tumour. Since tumour proliferative activity is mainly localised to its external zone, and taking into account that generation and expansion of genetic mutations depend on the number of cell divisions, important differences in gene expression between central and peripheral sections of the same tumour are to be expected. Here, we have studied variations in the genetic expression profile between peripheral and internal samples of the same brain tumour. We have carried out microarray analysis of mRNA expression, and found a differential profile of genetic expression between the two cell subsets. In particular, one major nuclear protein that regulates cell responses to DNA-damaging and stress signals, GADD45alpha, was expressed at much lower levels in the peripheral zone, as compared to tumour core samples. These differences in GADD45alpha mRNA transcription levels have been confirmed by quantitative analysis via real time PCR, and protein levels of GADD45alpha also exhibit the same pattern of differential expression. Our findings suggest that GADD45alpha might play a major role in the regulation of brain tumour invasive potential.

No AccessJournal of UrologyLetter to the editor/errata1 Apr 2007Re: Clinical and Immunological Characteristics of Patients With Serologic Progression of Prostate Cancer Achieving Long-Term Disease Control With Granulocyte-Macrophage Colony-Stimulating FactorB. I. Rini, L. Fong, V. Weinberg, B. Kavanaugh and E. J. Small J Urol 2006; 175: 2087–2091 Antonio Brú Antonio BrúAntonio Brú More articles by this author View All Author Informationhttps://doi.org/10.1016/j.juro.2006.11.050AboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareFacebookLinked InTwitterEmail "Re: Clinical and Immunological Characteristics of Patients With Serologic Progression of Prostate Cancer Achieving Long-Term Disease Control With Granulocyte-Macrophage Colony-Stimulating Factor." The Journal of Urology, 177(4), pp. 1585–1586 References 1 : Super-rough dynamics on tumor growth. Phys Rev Lett1998; 81: 4008. Google Scholar 2 : The universal dynamics of tumor growth. Biophys J2003; 85: 2948. Google Scholar 3 : Pinning of tumoral growth by enhancement of the immune response. Phys Rev Lett2006; 92: 238101. Google Scholar 4 : Regulation of neutrophilia by granulocyte colony-stimulating factor: a new cancer therapy that reversed a case of terminal hepatocellular carcinoma. J Clin Res2006; 8: 9. Google Scholar 5 : Transferable anticancer innate immunity in spontaneous regression/complete resistance mice. Proc Natl Acad Sci U S A2006; 103: 7753. Google Scholar 6 : Double-blind, placebo-controlled, randomized trial of granulocyte-colony stimulating factor during postoperative radiotherapy for squamous head and neck cancer. Cancer J2006; 12: 182. Google Scholar 7 : Phase II trial of GM-CSF + thalidomide in patients with androgen-independent metastatic prostate cancer. Urol Oncol2005; 23: 82. Google Scholar Departamento de Matematica Aplicada, Universidad Complutense, Madrid, Spain© 2007 by American Urological AssociationFiguresReferencesRelatedDetails Volume 177Issue 4April 2007Page: 1585-1586 Advertisement Copyright & Permissions© 2007 by American Urological AssociationMetricsAuthor Information Antonio Brú More articles by this author Expand All Advertisement PDF downloadLoading ...

This paper reports experimental results regarding the scaling properties of wetting fronts during the hydration of repacked bentonite clay with a wide range of pore sizes (over five decades). The process of hydration in this swelling, heterogeneous, porous medium was analyzed using a Hele–Shaw hydration cell. In highly disordered media, anomalous diffusion of the hydration interface and the effect of capillary forces are best understood using a volume filling structure model. This concept of porous media also allows the changes in the position of the mean position of the interface and the water volume intake over time to be explained. The change in the mean interface position follows the expression <h(x,t)>∝tγ with γ being time dependent until pinning occurs. This is the first report of the pinning of a water interface in a natural porous medium as a consequence of the medium heterogeneity and capillary force disorder produced by the randomness of its pore sizes. The hydration process produced interfaces with a characteristic roughness described by an exponent of 0.63. The results obtained from these experiments reveal a phenomenology unexplained by current theoretical models. The process cannot be classified into any known universality class of dynamics.

This paper describes some experiments on the manner in which external pressure affects cell colony growth in general, and tumour growth in particular. More precisely, our results show that cell colony borders growing under high-pressure conditions have geometrical and dynamical properties that are markedly different from those corresponding to growth under homeostatic, normal pressure conditions. These behaviours are characterized by means of the so-called dynamical exponents of each type of growth. These are shown to correspond to statistical properties of solutions of some stochastic partial differential equations that account for the evolution of the interface between the expanding colony and the surrounding medium.

Poster Presentationsincreased to around 50% after 72 h.Histology confirmed that slow, severe loading caused considerably more damage than fast, impact load with the presence of fissuring and uneven GAG distribution particularly in the deeper zones of the tissue.Conclusions: Although producing the same strain in the explant, fast, impact loading was less damaging to cartilage than severe loading that took almost 30 times longer to reach peak stress.Induction of apoptosis was more rapid with severe loading although similar levels were reached in both methods after 3 days in culture.The higher modulus, a measure of resistance to deformation, in the fast, impact loading may explain the increased ability of the cartilage to protect itself from damaging stress levels.The peak stresses reached in the fast, impact loading were more than 20 times that of the slow, severe load suggesting that stress alone is not a good indicator of damage.